A new study combines rodent optogenetics and 7T fMRI to map periaqueductal gray regulation, aiming to develop neurofeedback for PTSD.
Category: genetics – Page 4
New heart disease mechanism revealed: Next-generation targeted therapy shows benefit across mutation types
A study led by the Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC), working in collaboration with an international research team, has identified a new molecular mechanism involved in hypertrophic cardiomyopathy, the most common inherited cardiovascular disease.
The research, published in Nature Cardiovascular Research, also demonstrates that mavacamten—the first targeted therapy available for this condition—is effective across different types of genetic mutations.
Hypertrophic cardiomyopathy is the most common inherited heart disease and the leading cause of sudden cardiac death in young people and athletes.
Ultrasound-based pacemaker noninvasively steadies the heart
MIT engineers have developed a noninvasive pacemaker that stimulates the heart using ultrasound. The design could one day provide a surgery-free alternative to traditional cardiac implants.
The new device is designed as a small sticker that can be worn on the chest. Tiny transducers on the sticker send ultrasound pulses through the chest to stimulate the heart. The ultrasound waves trigger the opening of certain ion channels in heart cells, an effect the researchers amplified through genetic engineering. When the channels open, they let in calcium, which signals a heart cell to squeeze and beat.
In experiments in the lab, the researchers applied ultrasound waves to engineered human cardiac cells and found that the pulses effectively maintained the cells’ healthy contractions. They also tested the ultrasound sticker on rats and found the device quickly, safely, and noninvasively corrected arrhythmias and restored normal, regular heart contractions.
Inhibiting protein to treat myeloproliferative neoplasms shows preclinical promise
Inhibiting menin, a protein that supports leukemia growth and is already targeted to treat some forms of leukemia, also holds promise for treating myeloproliferative neoplasms. A new study from scientists at St. Jude Children’s Research Hospital showed that inhibiting menin significantly extended survival and reversed multiple disease features in preclinical models. The findings were published today in Cancer Cell.
Menin is best known as a therapeutic vulnerability in certain types of acute leukemia, including those with KMT2A gene rearrangements or NPM1 mutations. Menin inhibitors, such as revumenib, have greatly improved treatment for these cancers and are approved by the Food and Drug Administration (FDA). However, menin inhibition can reduce megakaryocytes (normal platelet-forming cells) and decrease platelet counts. Producing too many megakaryocytes is a hallmark of diseases called myeloproliferative neoplasms, which are slow-developing, rare blood cancers.
John Crispino, Ph.D., MBA, St. Jude Division of Experimental Hematology director and Department of Hematology member, tested whether inhibiting menin could be a viable therapeutic strategy for myeloproliferative neoplasms.
Can Mushrooms Reduce LDL? 53-Test Analysis
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Dr. David Sinclair: The First Human Trial of an Age-Reversal Therapy #podcast #lifespan #longevity
Harvard geneticist David Sinclair returns to explain how his lab’s age-reversal technology has moved from mice and primates into FDA-cleared human trials — starting with an attempt to reverse vision loss from glaucoma, a condition considered permanent. Sinclair breaks down the science of Yamanaka factors, why using three genes instead of four sidesteps the cancer risk, and his core thesis: make the body young enough and it can cure its own diseases.
He and James also go deep on the practical longevity playbook: NMN, NAD and Sirtuins, metformin and berberine, testosterone and muscle mass, sleep, diet, and how to separate real science from longevity misinformation. Sinclair shares his own protocol at 56, his 86-year-old father’s results, and teases a next-generation \.
This unusual epigenetic modifier promotes certain cancers but suppresses others
The epigenetic modifier MLL4 has an unassuming name—the 4, for instance, indicates it’s just one in a family of such modifiers. But MLL4 is quite special: In a specific type of leukemia, it drives disease progression, while in solid tumors, it acts as a suppressor.
The paradoxical nature of MLL4 made it a compelling enigma for Rockefeller University’s Robert Roeder, a pioneer in the field of genetic transcription. Now his Laboratory of Biochemistry and Molecular Biology at Rockefeller University has used a combination of biochemistry, genetics and structural biology to find surprising new characteristics of MLL4 that expand our understanding of its range of functions, including its relationship to a tumor-suppressing protein. The findings, published in Molecular Cell, could illuminate how the MLL4 complex helps switch genes on—including cancer genes in leukemia.
“This research demonstrates that MLL4 has functions in transcription that were entirely unknown before,” says Roeder. “And because MLL4 is a key regulator of gene activity, it’s important to understand how it works—especially in cancer cells.”
Genetic mapping identifies new hope for bone diseases
In a global breakthrough published in Nature Genetics, researchers have successfully mapped the cells and genes that regulate bone formation and loss at an unprecedented scale and discovered the critical role that blood vessel cells play in bone health.
By combining genomic sequencing with data from half a million individuals, the research team identified hundreds of previously unknown genes that govern bone health and revealed cells surrounding blood vessels as one of the drivers of bone repair—a role that has been underappreciated until now.
Led by Professor Peter Croucher and Dr. Ryan Chai from the Garvan Institute of Medical Research, Associate Professor John Kemp from Mater Research, and Professor Graham Williams and Professor Duncan Bassett from Imperial College London, the team’s findings fundamentally enhance our understanding of skeletal disease.
Epigenetic mapping provides deeper insight into leukemia
Researchers at Karolinska Institutet in Sweden and Kyoto University in Japan have identified new subgroups of the blood cancer acute myeloid leukemia. The study, published in the journal Nature, shows that changes in the regulation of genes within cells can help explain variation in the disease and influence prognosis and treatment choices.
Acute myeloid leukemia (AML) is an aggressive form of blood cancer in which immature blood cells grow uncontrollably. Despite extensive knowledge of the genetic alterations underlying the disease, it is still difficult to fully understand why patients develop different disease courses. In this study, the researchers analyzed so-called epigenetics—how genes are regulated without changes to the DNA sequence.